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Rigorous evidence of "what works" to improve health care is in demand, but methods for the development of interventions have not been scrutinized in the same ways as methods for evaluation. This article presents and examines intervention development processes of eight malaria health care interventions in East and West Africa. A case study approach was used to draw out experiences and insights from multidisciplinary teams who undertook to design and evaluate these studies. Four steps appeared necessary for intervention design: (1) definition of scope, with reference to evaluation possibilities; (2) research to inform design, including evidence and theory reviews and empirical formative research; (3) intervention design, including consideration and selection of approaches and development of activities and materials; and (4) refining and finalizing the intervention, incorporating piloting and pretesting. Alongside these steps, projects produced theories, explicitly or implicitly, about (1) intended pathways of change and (2) how their intervention would be implemented.The work required to design interventions that meet and contribute to current standards of evidence should not be underestimated. Furthermore, the process should be recognized not only as technical but as the result of micro and macro social, political, and economic contexts, which should be acknowledged and documented in order to infer generalizability. Reporting of interventions should go beyond descriptions of final intervention components or techniques to encompass the development process. The role that evaluation possibilities play in intervention design should be brought to the fore in debates over health care improvement.

Udgivelsesdato: 2010-Jan To estimate the weight deficit and body composition of cases of pulmonary TB (PTB), and assess the roles of HIV and the acute-phase response, a cross-sectional study was carried out in Tanzania. Weight, body mass index (BMI), arm muscle area (AMA), arm fat area (AFA) and the serum concentration of the acute-phase protein alpha(1)-antichymotrypsin (serum ACT) were evaluated for each of 532 cases of PTB and 150 'non-TB' controls. On average, the female cases of PTB not only weighed 7.8 kg less but also had BMI that were 3.1-kg/m(2) lower, AMA that were 14.8-cm(2) lower, and AFA that were 7.6-cm(2) lower than those seen in the female subjects without TB. Similarly, on average, the male cases of PTB weighed 7.1 kg less and had BMI that were 2.5-kg/m(2) lower, AMA that were 18.8-cm(2) lower and AFA that were 1.6-cm(2) lower than those seen in the male subjects without TB. Although HIV infection was associated with a 1.7-kg lower weight and a 0.6-kg/m(2) lower BMI (with deficits in both AMA and AFA) among males, it was not associated with any such deficits among the female subjects. Elevated serum ACT was found to be a negative predictor of BMI, AMA and AFA, partially explaining the effects of the PTB but not those of the HIV. There is need for a better understanding of the determinants and effects of loss of fat and lean body mass in HIV-positive tuberculosis.

In November-December 2002, stool samples from a random sample of the human population (N = 190) in the Garu area of northern Ghana were checked for intestinal helminths, using a single Kato smear and duplicate coprocultures for each subject. All 190 subjects were subsequently treated with a single, 400-mg dose of albendazole and 146 of them were successfully re-examined 21-28 days post-treatment. Prior to treatment, 75.5% of the Kato smears were found to contain 'hookworm-like' eggs (with a geometric mean egg count among the positives of 578 eggs/g faeces), and the third-stage larvae of Oesophagostomum bifurcum and hookworm were found in the cultures of stools from 34.2% and 77.4% of the subjects, respectively. Among the subjects who had positive Kato smears before treatment, albendazole treatment led to a cure 'rate' of 79.0% and an egg-reduction 'rate' of 73.5%. The results from the coprocultures indicated cure 'rates' of 98.0% for O. bifurcum but only 51.3% for hookworm. Only one subject was still positive for O. bifurcum after treatment. Among those still positive for hookworm after treatment, the larva-reduction 'rate' was 79.8%. The egg-/larva-reduction 'rates' among those with heavy infections prior to treatment were90%, whether the data analysed came from the Kato smears or the coprocultures. It may be concluded that a single dose of albendazole is very likely to cure an O. bifurcum infection and to reduce greatly the intensity (but not the prevalence) of any hookworm infections.

Ultrasonography has already revealed that up to 50% of individuals in some villages in northern Ghana have colonic pathology induced by Oesophagostomum bifurcum. Approximately 2% of those affected progress to clinical oesophagostomiasis if left untreated. In the present study, ultrasound-positive children living in a heavily infected community were each given 5 days of treatment with albendazole (10 mg/ kg.day), early in the dry season. Treatment reduced the prevalence, number, size and half-life of the ultrasound-visible nodules, stopped the excretion of O. bifurcum eggs, and reduced the development of clinical oesophagostomiasis during the subsequent 8 months. However, the treatment had no impact on the new infections that occurred during the following rainy season, and no impact on nodule prevalence by the end of that rainy season. Surgical management may not be essential in non-acute cases of clinical oesophagostomiasis, as albendazole may kill the nodule-dwelling worms.

Infection with Plasmodium falciparum is a major cause of anaemia in pregnancy, especially in primigravidae. Of 853 primigravidae visiting an antenatal clinic in Hoima district, western Uganda, for the first time, 530 (62.1%) were found to have P. falciparum parasitaemias and 305 (57.5%) of these had at least 1000 parasites/microliter blood. Plasmodium falciparum parasitaemia was significantly associated with anaemia (relative risk = 0.84, with 95% confidence limits = 0.74-0.96; P = 0.01). Malarial parasites were detected in80% of the women who had severe anaemia (P = 0.0008) and haemoglobin concentrations decreased with increasing intensity of infection (P = 0.03). Malarial hyper-reactive splenomegaly was associated with high parasite density (P = 0.01) and low haemoglobin level (P0.0001). Effective measures aimed at prevention of malaria and anaemia in pregnancy, especially in primigravidae, would significantly reduce anaemia and its deleterious effects on both the mother and the baby.

The purpose of this study was to investigate whether patients with chronic meningococcemia have abnormalities in their humoral immune system. The alternative and classical complement system, the levels of IgA, IgG and IgM, as well as IgG subclasses were studied in 15 individuals who had recovered from chronic meningococcemia. We found one individual with complete deficiency of properdin, a component of the alternative complement pathway. In the other patients, the complement system was normal. The mean plasma IgG concentration was significantly below normal in the patient group, while the mean values of IgA, IgM and the IgG subclasses were normal. Two individuals, however, had low IgG2 and IgG4 levels. We conclude that properdin deficiency and reduced plasma IgG levels may predispose to chronic meningococcal disease, but that the majority of patients with chronic meningococcemia have a normal humoral immune system.

We have examined 125 individuals who have earlier had meningococcal (mgc) disease. They belonged to one or more of the following groups: (1) 2 or more cases of mgc disease in the same family; (2) individuals with 2 episodes of mgc disease or with 1 episode of mgc disease and 1 or more episodes of purulent meningitis of another aetiology; and (3) infections with Neisseria meningitidis belonging to serogroups that are uncommon as causes of disease and presumably low-virulent (W-135, 29E, X, Y). Among these we found 15 complement (C)-deficient individuals (12%). The prevalence of C deficiency in the groups above was 7%, 41% and 19%, respectively. The first group (family cases), is very heterogeneous and may be further subdivided into 2 groups: families whose members fell ill within an interval of 30 days (in these the prevalence of C deficiency was 2%), and families in which the interval between mgc disease cases exceeded 30 days (in those the prevalence of C deficiency was 14%). We found a predominance of defects of the initiation pathways, with properdin deficiency being the most common.